International Mammalian Genome Society

The 16th International Mouse Genome Conference (2002)

Plenary Presentations * Oral Presentations *
Poster Presentations: Complex Genetics and Disease Modifiers * Developmental Genetics * Functional Genomics * Gene Discovery * Genetic Manipulations to Alter Gene Function * Mouse Models: Human Disease and Pharmacogenetics * Sequence Annotation and Comparative Analysis of Genomes *
Attendees * Sponsors * Table of Contents * Photographs * Awards

POSTER 179 - COMPARING MANUALLY ANNOTATED MOUSE AND HUMAN GENE CLUSTERS: THE XMHC AND PROLACTIN CLUSTERS

L Wilming
Wellcome Trust Sanger Institute

Peyrefitte S, di Bernardo D, Wilming L
Wellcome Trust Sanger Institute

The human extended Major Histocompatibility Complex (xMHC) region is located telomeric of the classical class I MHC region on chromosome 6p. In mouse most of the syntenic region is located on chromosome 13 (part of it is on chromosome 17 with the rest of the MHC cluster). We compare the mostly manually annotated regions on mouse and human genomic sequence. Not withstanding the fact that the various clusters and solitary genes between them are conserved in the same order, there is a considerable difference in the number of members in certain groups, such as the butyrophilin and vomeronasal receptor (Vnr) clusters. Indeed, our observation of seven new Vnr genes (in addition to the 15 known) in the mouse leads to the possibility that there the Vnr repertoire (involved in pheromone perception) is considerably larger than previously thought.Approximately 14 prolactin and prolactin-like genes are clustered on mouse chromosome 13 (telomeric of the xMHC). Comparison with the human genome reveals that again there is a significant disparity in the number of members, with humans having only around five homologous genes, four located in a cluster on chromosome 17 and only one member on syntenic chromosome 6. Proteins from the prolactin family are hormones involved in various aspects of pregnancy and lactation. Is this difference in prolactin gene number a reflection of physiological differences between rodent and primate pregnancies or did humans find a way to compensate for the reduced number of prolactin genes?